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C-reactive protein
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== Function == CRP binds to the [[phosphocholine]] expressed on the surface of bacterial cells such as pneumococcus [[bacteria]]. This activates the [[complement system]], promoting [[phagocytosis]] by macrophages, which clears [[necrotic]] and [[apoptotic]] cells and bacteria.<ref name="pmid34945133">{{cite journal | vauthors = Enocsson H, Karlsson J, Li HY, Wu Y, Kushner I, Wetterö J, Sjöwall C | title = The Complex Role of C-Reactive Protein in Systemic Lupus Erythematosus | journal = Journal of Clinical Medicine | volume = 10 | issue = 24 | page = 5837 | date = December 2021 | pmid = 34945133 | pmc = 8708507 | doi = 10.3390/jcm10245837 | doi-access = free }}</ref><ref name="Bray 2016"/> With this mechanism, CRP also binds to ischemic/hypoxic cells, which could regenerate with more time. However, the binding of CRP causes them to be disposed of prematurely.<ref name="pmid33679775">{{cite journal | vauthors = Sheriff A, Kayser S, Brunner P, Vogt B | title = C-Reactive Protein Triggers Cell Death in Ischemic Cells | journal = Frontiers in Immunology | volume = 12 | issue = | pages = 630430 | date = 2021 | pmid = 33679775 | pmc = 7934421 | doi = 10.3389/fimmu.2021.630430 | doi-access = free | url = }}</ref><ref name="pmid37626775">{{cite journal | vauthors = Sheriff A, Kunze R, Brunner P, Vogt B | title = Being Eaten Alive: How Energy-Deprived Cells Are Disposed of, Mediated by C-Reactive Protein-Including a Treatment Option | journal = Biomedicines | volume = 11 | issue = 8 | date = August 2023 | page = 2279 | pmid = 37626775 | pmc = 10452736 | doi = 10.3390/biomedicines11082279 | doi-access = free | url = }}</ref> CRP binds to the Fc-gamma receptor IIa, to which IgG isotype antibodies also bind.<ref name="pmid35806892">{{cite journal | vauthors = Sheriff A | title = Special Issue "C-Reactive Protein and Cardiovascular Disease: Clinical Aspects" | journal = Journal of Clinical Medicine | volume = 11 | issue = 13 | date = June 2022 | page = 3610 | pmid = 35806892 | pmc = 9267697 | doi = 10.3390/jcm11133610 | doi-access = free }}</ref> In addition, CRP activates the classical complement pathway via C1q binding.<ref name="pmid35333926">{{cite journal | vauthors = Buerke M, Sheriff A, Garlichs CD | title = [CRP apheresis in acute myocardial infarction and COVID-19] | language = German | journal = Medizinische Klinik, Intensivmedizin und Notfallmedizin | volume = 117 | issue = 3 | pages = 191–199 | date = April 2022 | pmid = 35333926 | pmc = 8951661 | doi = 10.1007/s00063-022-00911-x | url = }}</ref><ref name="pmid29706967">{{cite journal | vauthors = Sproston NR, Ashworth JJ | title = Role of C-Reactive Protein at Sites of Inflammation and Infection | journal = Frontiers in Immunology | volume = 9 | issue = | pages = 754 | date = 2018 | pmid = 29706967 | pmc = 5908901 | doi = 10.3389/fimmu.2018.00754 | doi-access = free | url = }}</ref> CRP thus forms immune complexes in the same way as IgG antibodies. This so-called [[acute phase response]] occurs as a result of increasing concentrations of [[interleukin-6]] (IL-6), which is produced by [[macrophage]]s<ref name=Pepys/> as well as [[adipocyte]]s<ref name="Lau"/> in response to a wide range of acute and chronic inflammatory conditions such as [[bacterial infection|bacterial]], [[viral infection|viral]], or [[fungal infection|fungal]] infections; [[rheumatic]] and other [[inflammatory disease]]s; [[malignancy]]; and tissue injury and necrosis. These conditions cause release of IL-6 and other [[cytokine]]s that trigger the synthesis of CRP and [[fibrinogen]] by the liver. CRP binds to phosphocholine on micro-organisms. It is thought to assist in [[Complement system|complement]] binding to foreign and damaged cells and enhances phagocytosis by macrophages ([[opsonin|opsonin-mediated phagocytosis]]), which express a receptor for CRP. It plays a role in [[innate immunity]] as an early defense system against infections.<ref name="Bray 2016"/> {{Clear}}
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